Dr. Ajayi completed his MD degree at Howard University College of Medicine and is currently completing his Hospice and Palliative Care fellowship in Aventura, Florida.
Dr. Cañizares-Otero completed her MD degree at St George’s University School of Medicine and is currently completing her Internal Medicine residency program in Aventura, Florida. She is interested in pursuing a pulmonary-critical care fellowship.
Abstract
Blast crisis and the associated hyperleukocytosis/leukostasis syndromes denote a medical emergency and require both rapid assessment and initiation of specific therapies. Any delays to the commencement of therapy are directly related to increased mortality in an already highly fatal condition. The mainstay of therapy is rapid initiation of supportive care and commencement of induction antineoplastic therapy. Leukapheresis and treatment with hydroxyurea, despite being quite common in clinical practice, are not the standard of care and do not carry with them any meaningful improvements in long-term mortality [1]. Leukostasis is an important aspect of the syndrome defined by hyperleukocytosis, occurring mainly in the sensitive tissue comprising lung parenchyma and cerebral vascular architecture. Two major theories exist to explain the mortality caused by said phenomenon: stasis in the microvasculature and massive cytokine release [2]. It has been noted that endothelial cells release massive cytokine cascades and signaling markers to attract even more blasts to a specific site, causing a systemic inflammatory reaction that seems to persist even after leukapheresis, with most cases of mortality being documented in the days to weeks following initiation of therapy and hospital admission [3]. This suggests there exists myriad other factors, many of them possibly unknown, which predispose individuals afflicted with this unfortunate illness to high mortality with little in the way of effective treatment.